Figure 1 Neuromyelitis optica spectrum disorder (NMOSD) subgroups and patients with relapsing-remitting multiple sclerosis (RRMS) show different antibody.

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Figure Seropositivity for IgG against HSV-1, CMV, and EBV
Figure 4 Neuromyelitis optica spectrum disorder brain lesions
Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.
Figure 3 Antibodies to MOG using different secondary antibodies: Anti-human IgG (H + L), IgG1, or IgM(A) Comparison of binding to full-length myelin oligodendrocyte.
Figure 3 Immunohistochemical analyses of positive and negative Epstein-Barr virus (EBV) control tissues using immunostaining Immunohistochemical analyses.
Figure 4 Correlation of age with [11C](R)-PK11195 binding in the normal-appearing white matter (NAWM) and thalami Correlation of age with [11C](R)-PK11195.
Figure 1 Percent positivity by clinical feature Overall, 6
Figure 3 JCV index changes in JCV+ patients
Figure 1 Flow diagram of the assays and the samples that were evaluatedA total of 1,109 samples were initially screened at a serum dilution of 1:20 for.
Figure 1 Effect of DMF therapy on T cell subsets
Figure 1 Integrative model of NMO/SD pathogenesis
Figure 2 Brain biopsy Brain biopsy (A) Double staining with anti-aquaporin-4 (AQP4) antibody (dark green) and Luxol fast blue (blue) is shown. Loss of.
Figure 2 Elevated antibody reactivities against myelin and Epstein-Barr virus (EBV) peptides in relapsing-remitting multiple sclerosis (RRMS) and higher.
Figure 1 MOR103 sequential-dose trial flowchart of study population with multiple sclerosis aPatients received 2 doses of study drug before trial withdrawal.
Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer
Figure 1 8-Iso-PGF2α levels in CSF of patients with MS and controlsCSF 8-iso-prostaglandin F2α (8-iso-PGF2α) levels were estimated using an ELISA. (A)
Figure 2 Exemplary MRI of a patient with contrast enhancement on postcontrast FLAIR MRI of a 54-year-old patient with viral meningitis caused by varicella-zoster.
Figure Association of hippocampal subfield volumes to cognition by neopterin level, volumes, and cognition adjusted for age, education, race, sex, and.
Figure 2. ROC curves for different group comparisons
Figure 1 Characteristics of the German National MS Cohort
Figure 2 JCV index JCV index (A) Fifty samples of natalizumab-treated patients with multiple sclerosis were assessed twice for their anti-JCV antibody.
Figure 2 Representative brain MRIs from patients with neuromyelitis optica Lesions are localized at sites of high aquaporin-4 expression (white dots).
Figure Family tree with the HLA haplotyping of 6 members of the family
Figure 4 Pattern of relapse in patients with MOG-Ab Five myelin oligodendrocyte glycoprotein antibody (MOG-Ab)–positive patients experienced a relapse,
Figure 1 The human adaptive immune profile in multiple sclerosis (MS)‏
Figure 4 Aquaporin-4 immunoglobulin G (AQP4-IgG) index in time-matched paired serum-CSF specimens: 3 attack/preattack pairs and 7 bridge/remission pairs.
Figure 1 JCV serostatus JCV serostatus (A) Serostatus of 1,921 natalizumab-treated patients with multiple sclerosis, with JCV− patients shown in black.
Figure 5 Pairwise correlations between selected patient-reported outcomes and performance tests in patients with MS (A) The number of pairwise correlations.
Figure 3 Longitudinal performance of 2 MS–cohabitant participant pairs on Ishihara color testing Both response speed and response accuracy are provided.
Figure 4 Confirmatory cohorts to assess MOG-IgG1 assay(A) All 81 aquaporin-4 (AQP4)- seropositive patients (blue) from the Oxford National neuromyelitis.
Figure Clinical and radiologic course(A) The T2 contrast-enhanced sequence on day 3 shows an extensive central cord lesion extending from C2 to T7. Clinical.
Figure 1 Kaplan-Meier estimation of time to neuromyelitis optica (NMO) conversion and development of motor disability Kaplan-Meier estimation of time to.
Figure 1 Phenotype and functional properties of B cells in MS and HCs at baseline Phenotype and functional properties of B cells in MS and HCs at baseline.
Figure 1 Annual trend in specimen type submitted as first sample for aquaporin-4 immunoglobulin G testing (serum only vs CSF only vs both) from 101,065.
Figure 3 Correlation of lipid indexes to MRI measures of disease severity in multiple sclerosis Correlation of lipid indexes to MRI measures of disease.
Figure 2 Reduced frequency of central memory CD4 T cells in patients with PML Reduced frequency of central memory CD4 T cells (CD4Tcm) (p < ), naive.
Figure 1 Examples illustrating gating strategy for fluorescence-activated cell sorting (FACS)‏ Examples illustrating gating strategy for fluorescence-activated.
Figure 2 Immunohistological detection of EBV latent and early lytic proteins in MS and control brains Immunohistological detection of EBV latent and early.
Figure Varicella-zoster virus antigen in the temporal artery, aorta, and carotid artery of a patient with refractory giant cell arteritis Immunohistochemical.
Figure 2 Spectrum of abnormal CT scanning of patients with bacterial meningitis presenting with a minimal Glasgow Coma Scale score Spectrum of abnormal.
Figure 1 Anti-Epstein-Barr virus nuclear antigen-1 IgG quartile antibody status differences in MRI measures Anti-Epstein-Barr virus nuclear antigen-1 IgG.
Figure 1 BG-12 treatment reduced total circulating B cells and had variable effects on memory B cells BG-12 treatment reduced total circulating B cells.
Figure 2 Correlation of CSF 8-iso-PGF2α levels with other indicators of oxidative stressCorrelations of 8-iso-prostaglandin F2α (8-iso-PGF2α) values with.
Figure 1 Patterns of study retention The proportion of individuals actively participating in the study is displayed over the course of the study. Patterns.
Figure 4 Alemtuzumab-mediated effects on interleukin (IL)–23 and granulocyte-macrophage colony-stimulating factor (GM-CSF) production in innate myeloid.
Figure 3 Pedigrees of 3 multiplex families with NLRP3 mutations and MS The patient numbers refer to the patients listed in table 1. Pedigrees of 3 multiplex.
Figure Overview of patients with demyelinating diseases, presence of clinical symptoms frequently associated with NMDAR encephalitis, and antibody status.
Figure 1 CD52 expression on innate myeloid and lymphoid cell subsets
Figure 1 Representative spinal cord MRIs from patients with neuromyelitis optica Longitudinally extensive transverse myelitis of the cervical (A) and cervicothoracic.
Figure 2 Correlation between wGRS and age at onset The figure shows the correlation between weighted genetic risk score (wGRS) and age at onset in all.
Figure 2. Detection of KIR4.1 autoantibodies using LIPS
Figure 1. Heat map of antibody binding patterns to glycolipid targets in Guillain-Barré syndrome (GBS) cases and controls Heat map of antibody binding.
Figure 4. The N:M ratio is significantly increased in patients with ALS and correlates with disease progression The N:M ratio is significantly increased.
Figure 1 Full-length MOG cell-based assay using a serum dilution of 1:160 as a cutoff for positivity (red line in both plots)(A) Myelin olidgodendrocyte.
Figure Avidity of IgG specific for influenza A and B following flu vaccinationAvidity of immunoglobulin (Ig) G specific for influenza A and B before and.
Figure 2 Frequency of the proportion of total WMLs with central veins in PPMS, RRMS, and SVD Frequency of the proportion of total WMLs with central veins.
Figure 1 Peripheral blood lymphocyte counts during dose titrationB-lymphocyte (CD19+; A) and total lymphocyte (CD45+; B) counts (cells/µL) in peripheral.
Figure 3 Impact of short-term MP administration on frequency and phenotype of slanDCs and monocytes in the blood of patients with MSThe percentages of.
Figure 2 Assessment of fluctuation in fatigue scores using environmental data The relationship between fatigue (as measured by the Modified Fatigue Impact.
Figure 3 Fluorescence-activated cell sorting (FACS) employing cells singly transfected with M1-AQP4 or M23-AQP4 or cotransfected with both AQP4 isoforms.
Figure 6 Multiple target epitopes exist in the N-terminal domains of Caspr2 (A) Multidomain deletion constructs of Caspr2 were generated to determine which.
Figure 3. Sensitivity and specificity of microarray analysis in relation to target number Sensitivity and specificity of microarray analysis in relation.
Figure 3 Alemtuzumab-induced changes in monocytes
Figure 3 C5B3 blocked MAC formation
Figure 5 C5B3 inhibited inflammatory infiltration in an NMOSD mouse model in vivo C5B3 inhibited inflammatory infiltration in an NMOSD mouse model in vivo.
Figure 1 Numbers/seropositivity rates of IVIg-naive and IVIg-exposed STRATIFY-2 enrollees* = % of enrollment samples, ** = date of IVIg and/or concentration.
Figure 4 C5B3 decreased NMOSD mouse model lesions in vivo
Figure 2. Percentage of CD16− monocytes in the blood is reduced during disease progression Percentage of CD16− monocytes in the blood is reduced during.
Figure 4 Illustration of a practice effect by examining longitudinal performance measures in patients with MS and cohabitants (A) Response time for each.
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Figure 1 Neuromyelitis optica spectrum disorder (NMOSD) subgroups and patients with relapsing-remitting multiple sclerosis (RRMS) show different antibody signatures Neuromyelitis optica spectrum disorder (NMOSD) subgroups and patients with relapsing-remitting multiple sclerosis (RRMS) show different antibody signatures Heat maps (A: RRMS [blue] vs aquaporin-4 antibody [AQP4Ab]+ NMOSD [red]; B: RRMS [blue] vs AQP4Ab− NMOSD [purple]; C: AQP4Ab+ NMOSD [red] vs AQP4Ab− NMOSD [purple]). The top 20 peptides from all pairwise subgroup comparisons as well as all AQP4 peptides are shown as rows (see key for peptides). Patients from the different subgroups are shown as columns (see key for patient groups). The color (see key for z score) indicates the intensity of the peptides standardized to the healthy controls, with blue indicating an upregulation and red a downregulation of peptide reactivities, given in standard deviations. Heat maps show a clustering of RRMS and AQP4Ab+ NMOSD (A) as well as RRMS and AQP4Ab− NMOSD (B), suggesting different antibody signatures in these patient groups. In contrast, such a clustering is not evident comparing the 2 NMOSD subgroups (C). CMV = cytomegalovirus; EBV = Epstein-Barr virus; VZV = varicella-zoster virus. Imke Metz et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e204 © 2016 American Academy of Neurology